Athena Vale
The human heart is an incredible organ, expanding and contracting non-stop throughout our entire lives. Unlike other muscles in the body, the heart never rests, and cardiac muscles are resistant to fatigue. This is because cardiac muscle contains more mitochondria than skeletal muscle, which act as power plants, generating adenosine triphosphate (ATP) for the transfer of chemical energy. However, recent research has indicated that extreme endurance exercise over a lifetime may cause fibrosis or scarring within the heart muscle, which can contribute to irregular heart function and eventually, heart failure.
| Characteristics | Values |
|---|---|
| Reason for cardiac muscle fatigue | Excessive stimulation, hypersensitive excitation-contraction coupling, or diminished performance capacity |
| Cause of muscle fatigue | Impaired sarcoplasmic reticulum (SR) Ca-transport activity |
| Effect of pacing-induced fatigue and halothane-induced MH | Reduction of Ca-sequestration activity of muscle homogenates |
| Cardiac muscle type | Striated |
| Cardiac muscle energy source | Mitochondria |
| Cardiac muscle fatigue resistance | High |
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What You'll Learn
Cardiac muscle is resistant to fatigue
The human body has three types of muscles: skeletal, smooth, and cardiac. Unlike skeletal muscles, which are attached to bones and tendons, the cardiac muscle is made of special cells called cardiomyocytes. These cells are joined together at adherens junctions, enabling the heart to contract forcefully without ripping.
The stimulus to make the heart pump comes from within and passes from fiber to fiber through gap junctions. This creates a synchronous wave that sweeps from the atria down through the ventricles and pumps blood out of the heart. Even if the nerves are destroyed, as in a transplanted heart, the heart continues to beat. This intrinsic rate can be modulated by the autonomic nervous system, which can increase or decrease the strength of the heartbeat.
While the heart is resistant to fatigue, cardiac fatigue can occur in athletes who perform extreme workouts over a long period. Recent research indicates that a lifetime of endurance athletics can lead to fibrosis or scarring within the heart muscle, which can contribute to irregular heart function and eventually heart failure. However, a single instance of endurance exercise is unlikely to cause permanent damage, and evidence suggests that endurance exercise is good for heart health.
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The cardiac muscle is made up of cardiomyocytes
The human body is composed of three types of muscles: skeletal, smooth, and cardiac. Cardiac muscle, also called the myocardium, is one of the three major categories of muscles found within the human body. The cardiac muscle is made up of cardiomyocytes, also known as cardiac muscle cells. These cells are responsible for the contractility of the heart and its pumping action. Each cardiomyocyte contains a single, centrally located nucleus surrounded by a cell membrane called the sarcolemma. The sarcolemma contains voltage-gated calcium channels, which are specialized ion channels that skeletal muscles do not possess.
Cardiomyocytes are striated, branched, and contain many mitochondria. They are under involuntary control, meaning they contract and expand in response to electrical impulses from the nervous system. The cardiac muscle cells contain branched fibers connected via intercalated discs that contain gap junctions and desmosomes. These interconnections allow the cardiomyocytes to contract together synchronously, enabling the heart to work as a pump. The gap junctions between adjacent cardiomyocytes allow for the propagation of coordinated action potentials from one cell to the next, a phenomenon known as electrical coupling.
The functional unit of cardiomyocyte contraction is the sarcomere, which consists of thick (myosin) and thin (actin) filaments. These filaments interact to form the basis of the sliding filament theory. The regular organization of myofibrils into sarcomeres gives cardiac muscle cells a striped or striated appearance when viewed under a microscope. These striations are caused by lighter I bands composed mainly of actin and darker A bands composed primarily of myosin. The sarcomeres are the fundamental contractile units of muscle cells, allowing the cardiac muscle to contract with enough force to supply blood to the entire body.
Cardiac muscle cells contain T-tubules, or transverse tubules, which are pouches of cell membrane that run from the cell surface to the cell's interior. T-tubules improve the efficiency of contraction and play a role in excitation-contraction coupling, action potential initiation, and regulation. While cardiac muscle fatigue due to exhaustive exercise has been observed, it is important to note that the high number of mitochondria in cardiac muscle cells provides a large amount of energy, making them highly resistant to fatigue.
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Cardiomyocytes have a high density of mitochondria
The human body has three types of muscles: skeletal, smooth, and cardiac. Skeletal muscles are attached to bones and tendons and control most voluntary body movements. Cardiac muscle, like skeletal muscle, is striated, and its cells are joined together at adherens junctions, enabling the heart to contract forcefully.
Cardiac muscle derives its energy from mitochondria within its cells, and the more mitochondria, the greater the available energy for the muscle. Cardiomyocytes have a high density of mitochondria, which are central to the maturation process of cardiomyocytes. During embryonic and fetal development, the developing embryo or fetus is exposed to changing nutrient, oxygen, and hormone levels. Mitochondria respond to these metabolic changes and transition from small, fragmented mitochondria to large organelles capable of producing enough ATP to support the contractile function of the heart.
Mitochondria also undergo maturation during the perinatal window, transitioning from small, fragmented organelles to large networks with developed cristae capable of the high oxidative capacity needed to produce enough ATP to support the contractile function of the heart. This maturation process is likely not merely a response to overall cardiomyocyte maturation; instead, mitochondria may be mediators of the molecular processes triggering maturation of cardiomyocytes.
Research has shown that giant mitochondria are frequently observed in different disease models within the brain, kidney, and liver. In cardiac muscle, these enlarged organelles are present across diverse physiological and pathophysiological conditions, including aging and exercise, and clinically in alcohol-induced heart disease and various cardiomyopathies. This mitochondrial aberration is widely considered an early structural hallmark of disease leading to adverse organ function.
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The process of contraction and relaxation
Calcium ions play a crucial role in the contraction process. When calcium enters the sarcoplasm, it binds to cardiac troponin-C, displacing tropomyosin and exposing the actin-binding sites. This activation of troponin-C by calcium ions is known as the cross-bridge cycling mechanism, which leads to the interaction between actin and myosin filaments. The force of contraction is determined by the length of the sarcomeres, which influences the formation of actin-myosin cross-bridges. The longer the sarcomeres, the greater the overlap between thick and thin filaments, resulting in a stronger contraction.
During relaxation, calcium ions are removed from the sarcoplasm. This removal is facilitated by two primary mechanisms: the exchange of three Na+ ions for one Ca++ ion and the utilisation of ATP to pump Ca++ across the sarcolemma. The reuptake of calcium ions into the SR results in a decrease in calcium concentration, leading to the termination of contraction. Tropomyosin, influenced by the phosphorylation of troponin I, returns to its resting position, blocking the interaction sites between actin and myosin filaments, thus allowing the muscle to relax.
The speed of contraction and relaxation is a critical factor in cardiac performance. A reduced speed of contraction and relaxation is often observed in cardiomyopathies, particularly those with diastolic dysfunction. Additionally, the forcefulness of contraction is important, and it is influenced by factors such as the initial length of the sarcomeres and the intracellular calcium concentration.
While the exact causes of muscle fatigue are not fully understood, it is associated with a decrease in muscle contraction. Fatigue may be influenced by reduced ATP reserves, accumulation of hydrogen ions and inorganic phosphate, and imbalances in Na+ and K+ levels, which can disrupt calcium regulation.
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Sarcoplasmic reticulum Ca-ATPase (SERCA) pumps
The human body has three types of muscles: skeletal, smooth, and cardiac. The cardiac muscle is unique in that its cells are joined together strongly at adherens junctions, enabling the heart to contract forcefully without the muscle fibres ripping apart. The stimulus for the heart to pump comes from within and passes from fibre to fibre through gap junctions.
Cardiac muscle fatigue can be caused by excessive stimulation, hypersensitive excitation-contraction coupling, or diminished performance capacity. This can lead to sarcoplasmic reticulum failure, which is associated with impaired Ca-transport activity. The SarcoEndoplasmic Reticulum Calcium ATPase (SERCA) pump is a key regulator of cellular calcium homeostasis. SERCA actively transports calcium ions from the cytosol back to the sarcoplasmic reticulum (SR) following muscle contraction. SERCA function is closely associated with muscle health and function, and SERCA activity is susceptible to muscle pathogenesis.
In the heart, SERCA pump activity is regulated by two small molecular weight proteins: phospholamban (PLB) and sarcolipin (SLN). PLN is found to be expressed in all muscle types but primarily interacts with the SERCA 2a isoform in cardiac and slow-twitch muscles. PLN inhibits SERCA activity by reducing the SERCA pumps' affinity to Ca2+, decreasing ATPase activity. Decreases in the expression levels of SERCA2a have been observed in a variety of pathological conditions, including heart failure.
SERCA stimulation has been investigated as a potential therapeutic method for the treatment of muscle pathologies. For example, interventions include the activation of SERCA activity and the genetic overexpression of SERCA. In addition, the effects of neuronal SERCA stimulation on improving neurodegenerative disorders have also been studied. For instance, the stimulation of neuronal SERCA in Alzheimer's disease can increase the ER Ca2+ store, leading to less influx of extracellular calcium to the cytosol of neuro cells, which can help regulate the production of amyloid-beta.
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Frequently asked questions
No, cardiac muscles are resistant to fatigue.
Cardiac muscles are made of cardiac muscle, consisting of special cells called cardiomyocytes. Unlike other muscle cells in the body, cardiomyocytes are highly resistant to fatigue. This is because they contain a high density of mitochondria, which skyrockets their energy output.
Cardiomyocytes are the individual cells that make up the cardiac muscle. The primary function of cardiomyocytes is to contract, which generates the pressure needed to pump blood through the circulatory system.
